Exercise Protects against Chronic β-Adrenergic Remodeling of the Heart by Activation of Endothelial Nitric Oxide Synthase

• DOI: 10.1371/journal.pone.0096892
• Publication Date: 2014-05-08T22:12:57Z
• Authors: Liang Yang; Zhe Jia; Lei Yang; Mengmeng Zhu; Jincai Zhang; Jie Liu; Ping Wu; Wencong Tian; Jing Li; Zhi Qi; Xiangdong Tang
• Keywords: Endothelial NOS

Extensive data have shown that exercise training can provide cardio-protection against pathological cardiac hypertrophy. However, how long the heart retain cardio-protective phenotype after cessation of is currently unknown. In this study, we investigated time course loss and signaling molecules are responsible for possible sustained protection. Mice were made to run on a treadmill six times week 4 weeks then rested period 0, 1, 2 followed by isoproterenol injection 8 days. Morphological, echocardiographic hemodynamic changes measured, gene reactivation was determined real-time PCR, expression phosphorylation status several analyzed Western-blot. HW/BW, HW/TL LW/BW decreased significantly in (ER) mice. The less necrosis lower fetal induced also found ER β-adrenergic overload attenuated protective effects be at least training. Western-blot analysis showed alterations endothelial nitric oxide synthase (eNOS) (increase serine 1177 decrease threonine 495) continued whereas increases Akt mTOR disappeared. Further study L-NG-Nitroarginine methyl ester (L-NAME) treatment abolished ER. Our findings demonstrate stimulation eNOS mice through provides acute cardioprotection